BMD 115 Test two
Terms in this set (282)
integrated system of small organs exerting large effects on cellular metabolic activity by hormonal means
bloodborne chemical substances functioning as signaling (messenger) molecules.
-Effects are seen far away from releasing organ. -Either stimulate or inhibit a target tissue's growth and/or function
-Effects can last from seconds to days
Neuroendocrine organ producing/releasing several hormones.
*Major endocrine controller ("The Boss")
*Also controls the ANS
Produced by several other tissues (adipose cells, small intestine, stomach, kidneys, heart).
-Not "true hormones" since action occurs close to site produced
exert their effects on same cells secreting them
exert their effects on cells that are nearby to those secreting them
Sweat, salivary glands, digestive juices.
-Non-hormonal substances are secreted through excretory ducts directly into
areas where they have their action.
Pituitary, thyroid, parathyroid, adrenal, pineal.
-Hormones are released into interstitial fluid, taken into blood, delivered to
mixed (endo/exocrine functions)
pancreas, gonads, placenta
Most body cells are hormone targets in regulating growth, maintenance and/or repair mechanisms.
-Growth and repair is always above maintenance.
-regulate metabolic activity of other cells.
-most exhibit lag (delay) times (secs-> hrs)
-mostly have prolonged (lasting) effects
amino acid-based (hormones)
hormones are protein hormones.
-amines, short chain peptides, long polypeptides
cholesterol-based hormones (e.g., corticosteroids)
biologically active lipids with local "hormone-like" activity released by nearly all cell membranes
Water soluble so they cannot directly pass through cell membranes, except for
-uses an internal messenger to relay an external signal (a plasma membrane)
Lipid soluble so they can readily pass through target cell membranes.
-cholesterol base enables hormone to pass through hydrophobic region of plasma membrane.
Target cell effects of hormones
plasma membrane permeability
(promote anabolic reactions)
enzyme systems (turns it on or off)
(causes substance release)
(supports maintenance, growth, &/or repair)
bind to external receptors, indirectly activates cells
Bind to internal receptors, directly activates cells.
-complexes w/ internal receptor protein, migrates to nucleus, & binds directly to DNA recognition site
-DNA binding stimulates transcription
Target Cells Specificity
Hormones circulate through bloodstream to most body tissues, excluded from brain by blood-brain barrier.
-Only activate target cells expressing their hormone receptor.
attractive force/binding strength
relative number of target cell receptors
hormone blood levels
increasing blood hormone concentration causes a corresponding increase in membrane receptor numbers. Only in peptide receptors.
continuously high levels of circulating hormone causes a decrease in receptor numbers. Too much hormone causes target tissue overstimulation. Only in peptide receptors.
Down-regulation prevents "over responsiveness" by desensitizing target cells, which respond less vigorously to hormone still present.
Steroid/thyroid hormones attach to blood carrier proteins.
Free (unbound) Hormones
Most peptide hormones lack carrier proteins.
reflect hormone rate of release & speed of inactivation/body removal
Length of time required for a hormone level in bloodstream to decrease by 50%. Half the hormone is in the blood and half is in the target organ.
-H2O-soluble = seconds
-lipid-soluble = hours to days
One hormone cannot exert full effects without another hormone being present.
one hormone's effects are multiplied in presence of another hormone (effects on a target cell are additive)
one or more hormone(s) oppose action of another hormone
secreted in direct response to changing ion/nutrient blood levels (concentration effect)
Direct nerve fiber innervation stimulates release.
1st endocrine organ hormone causes another organ to produce & release its own hormone
Synthesis/release is controlled by
negative feedback systems
unusual bi-lobed gland composed of two different tissues, secretes 8 major peptide hormones. Connected to hypothalamus by a stalk-like infudibulum.
neurohypophysis (posterior lobe of pituitary)
Composed of neural tissue originating in hypothalamus. Stores/releases hypothalamic-produced peptide hormones.
Does Not synthesize any hormones... Only stores/secretes them.
adenohypophysis (anterior lobe)
- composed of glandular tissue not originating in hypothalamus
-produces/secretes several peptide hormones
Neurohypophysis (posterior pituitary)
Downward growth of brain hypothalamic neural tissue.
- stores/releases two hypothalamic peptide neurohormones
-Oxytocin, antidiuretic hormone (ADH)
Neural transport pathway for delivery of oxytocin/ADH to posterior pituitary.
Adenohypophysis (anterior pituitary)
Upward growth of oral mucosa w/ no direct hypothalamic contact.
-synthesize/release 6 peptide hormones:
Growth hormone (GH), thyroid stimulating hormone (TSH), adrenocorticotrophic hormone (ACTH), follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL)
hypophyseal portal system
local blood capillary system linking hypothalamus w/ anterior pituitary
-used by hypothalamic hormones to reach/stimulate anterior pituitary
stimulate hormone synthesis/release
-Example: growth hormone releasing hormone (GHRH)
shut off hormone synthesis/release
-Example: growth hormone inhibiting hormone (GHIH)
are released, which, in turn, stimulate other endocrine glands to produce additional hormone(s).
-thyroid-stimulating hormone (TSH)
-adrenocorticotropic hormone (ACTH)
-follicle-stimulating hormone (FSH), luteinizing hormone (LH) both being gonadotropins.
All hypothalamic regulatory hormones are...
One joker in the deck. Its does not have an external receptor but an internal one. Peptide hormone but acts like a steroid hormone.
thyroid stimulating hormone (TSH)
stimulates normal thyroid development/secretory activity
hypothalamic thyrotropin-releasing hormone (TRH)
triggers thyroid stimulating hormone (TSH)
-produced by anterior pituitary somatotropic cells, mobilizes stored fat while conserving glucose
-feedback is regulated by antagonistic hypothalamic hormones
anabolic hormone functions
1. increases body cell size/cell division (most cells)
2. promotes bone/skeletal muscle (major targets) protein synthesis
3. ↑ synthesis of growth-promoting insulin-like growth factors (IGF) or somatomedins
Adrenocorticotropic Hormone (Corticotropin)
-produced by anterior pituitary corticotrope cells
-release is triggered by hypothalamic corticotropin-releasing hormone (CRH) in a daily rhythm
-stimulates adrenal cortex to release corticosteroids, like glucocorticoids
Levels of cortisol vary during the day. Cortisol levels are up when you are and down when you aren't.
Gonadotropins: FSH & LH
-both hormones stimulate male/female gonads but are absent in bloodstream of pre-pubertal boys/girls
-release is triggered by hypothalamic gonadotropin-releasing hormone (GnRH) during/after puberty
-both FSH/LH regulate ovaries/testes activity but FSH alone stimulates gamete production
lack of sex hormones. results in infertility.
-present in both males & females, blood levels rise rapidly in ♀ toward end of pregnancy
-levels controlled primarily by prolactin inhibiting hormone (PIH)
-stimulates female breast milk production
-important in cyclical actions such as ovulation/menstruation & immunity
Prolactin inhibiting hormone
is constantly secreted not allowing prolactin to be released. PIH must decrease for PRL to be released.
antidiuretic hormone (ADH)
influences water balance. (Retains water)
high blood solute levels (↑ osmolarity) - ADH release stimulates more water retention (< H2O loss)
low blood solute levels (↓ osmolarity) - ADH is not released, causes more water elimination (> H2O loss)
stimulates breasts/uterine smooth muscle contraction
2 hypothalamic hormones in posterior pituitary
antidiuretic hormone and oxytocin
prepartum of oxytocin
uterine/cervical stretching during late pregnancy produces more oxytocin receptors (up regulation)
postpartum of oxytocin
breastfeeding "triggers" continued oxytocin release causing milk ejection ("letdown" reflex)
synthetic oxytocin given to enhance uterus contractions
sense a change in blood solute conc. signals posterior pituitary to secrete ADH to avoid dehydration
Largest endocrine gland, anterior neck position, 2 lateral lobes connected by an isthmus or median tissue mass
produce thyroglobulin, a thyroid hormone precursor protein
produce another hormone called calcitonin
Thyroid Hormone (TH)
Major metabolic hormone controlling glucose oxidation, increased metabolic rate, heat production
TH is a peptide hormone, mixture of two closely related iodine-containing compounds:
1. triiodothyronine (T3)
2. thyroxine (T4)
Functions of thyroid hormone
helps maintain blood pressure
helps regulates tissue growth
skeletal & nervous system development
maturation & reproduction
Thyroid Hormone (TH) Synthesis
thyroid follicle lumens store tyrosine-containing thyroglobulin
"trapped" iodine (I-) becomes associated with thyroglobulin's tyrosine molecules in one of two ways, forms 2 TH precursors
T3/T4 result from an assembly of both MIT & DIT precursors
T3/T4 are released into bloodstream
1 MIT + 1 DIT =
1 DIT + 1 DIT=
rising blood T4 levels shuts off TSH/TRH release
tissues can convert T4 → T3 by removing one iodine atom
Thyroid Gland: Calcitonin
-Peptide hormone produced by thyroid parafollicular cells*
-Stimulus for release is a rise in blood Ca2+ levels
-Exhibits "bone sparing" effect at levels higher than normal
1. stimulates blood calcium uptake & storage by bone matrix
2. inhibits osteoclast activity to reduce bone resorption
four pea-size, yellow-brown glands usually located on posterior thyroid
peptide hormone produced by parathyroid gland chief cells
-Stimulus for release is a fall in blood Ca2+ level
-a calcitonin antagonist
a lot of cells
PTH (parathormone) body targets
1. bone - activates osteoclasts to digest matrix
2. kidney - promotes increase in blood Ca2+ reabsorption, activates more vitamin D, excretes phosphates
3. intestine - vitamin D activation to calcitrol Ca2+ absorption from food
- paired, pyramid-shaped organs sitting atop each kidney (renal gland)
structurally/functionally considered to be two separate glands since cortical/medullary areas produce different hormones
- outer glandular tissue makes up bulk of adrenal gland
-mediates long-term stress response, stimulated by ACTH released by anterior pituitary*
-inner nervous tissue in the adrenal gland, acts as part of ANS sympathetic division.
-mediates short-term stress response, stimulated by sympathetic preganglionic neurons
3 layers of adrenal cortex
mineralocorticoids, primarily aldosterone.
glucocorticoids, primarily cortisol.
(Looks like sticks, middle layer)
gonadocorticoids, primarily androgens
regulate extracellular fluid electrolyte concentrations by maintaining water/mineral balance (aldosterone)
-released aldosterone maintains Na+ balance
-secretion is stimulated by decrease in BP, increase in K+, increase in ACTH, renin release
keeps blood sugar levels relatively constant (cortisol)
-ACTH mostly stimulates cortisol production
-double increase during physical/emotional stress, strenuous activity, infection, injury to mobilize stored carbohydrates/lipids
Gonadocorticoids (sex hormones)
promotes puberty onset, secondary sex characteristics, sexual drive (androgen)
-before puberty weak adrenal androgens are converted to low levels of male testosterone & female estrogens.
-after puberty most sex hormones are produced by ovaries/testes
a lack of sexual identity
Principal body site where tyrosine is converted into catecholamines by medullary chromaffin cells
- Involved in many short-term stress responses
physical or emotional
potent heart/metabolic activity stimulator
blood vessel constriction to increased blood pressure
precursor of both epinephrine & norepinephrine
Mixed exocrine/endocrine gland located behind stomach
-Scattered pancreatic islets contain two major cell types producing hormones w/ antagonistic (opposite) effects
1. alpha cells - produce glucagon
2. beta cells - produce insulin
exocrine products by pancreas
digestive enzymes produced by acinar cells
endocrine products by pancreas
glucose regulatory hormones produced in islets of Langerhans
potent hypoglycemic agent, increase blood glucose levels when excess blood sugar is present.
-enhances glucose transport into tissue cells
-stimulates glucose conversion to its storage form = glycogen
potent hyperglycemic agent, blood glucose when low
-major target is stored liver glycogen
-cortisol also stimulates glucose formation from stored lipids (fats)
Paradoxical nature of blood
it can simultaneously exist in two different forms in same area: liquid and solid
liquid form of blood
flows inside circulatory vessels providing nutrients/oxygen to body cells while removing cellular wastes
solid form of blood
rapidly changes from a liquid to solid state to prevent further blood loss
excessive solid form =
excessive liquid form =
blood loss (hemorrhage)
Continuous, uninterrupted blood flow starting at heart continues through living vessels composed of endothelium
moves blood away from heart through series of highly-branching
blood reaches body tissues through nearby microscopic...
returns to heart, moves on to lungs, & then back to heart to start another circuit.
what kind of circuit does blood have to travel in?
pressures are equalized
blood loss only stops when?
what is the bodies only fluid tissue composed of a plasma fluid matrix that contains cellular elements
water, soluble proteins*, electrolytes, chemicals
erythrocytes = red blood cells (RBC's)
leukocytes = white blood cells (WBC's)
thrombocytes = platelets
The amount of red blood cells the body requires.
Relative percentage of RBCs (x%) when compared to total whole blood volume (100%).
separates blood into components = plasma, white blood cells + platelets (buffy coat), red blood cells
expected high & low values from a normal patient population, can vary by sex & age
males > females
infants > adults
1. physical - sticky, opaque fluid with a metallic taste (Na+)
2. viscosity - formed elements make it 5x denser than water
3. color - whole blood ranges from scarlet oxygen-rich blood to dark red oxygen-poor blood while plasma is straw colored
4. pH = slightly alkaline, from 7.35-7.45 (a very narrow range)
5. temperature = 38C, being slightly higher than body temp.
6. percentage body weight = approx. 8%
7. volume (mass-related):
a. healthy males = avg. 5-6 L (1.5 gal)
b. healthy females = avg. 4-5 L
transfer (O2 /nutrients), metabolic wastes (CO2 /urea), hormones from endocrine glands to target organs
body temperature (absorb/distribute heat), maintain normal pH (HC03-), preserve fluid volume between body compartments
prevent blood loss by activating platelets & coagulation proteins to initiate clot formation in both unbroken & broken blood vessels
Makeup constantly changes as substance exchange takes place at blood-interstitial fluid interface
blood plasma components
1. water (solvent) - 90% of blood plasma
2. dissolved substances (solutes) - >100 make up remaining 10%
proteins (albumin, gamma globulins, fibrinogen, enzymes, etc.)
non-protein nitrogen (blood urea nitrogen)
organic nutrients (glucose, fatty acids, vitamins)
electrolytes (most abundant solutes)
respiratory gases (O2 /CO2)
hormones (carrier bound-peptides/free hormones)
loses nucleus/organelles before leaving marrow spaces. Present in blood stream for 110-120 days
-Complete cells since leukocytes retain their nucleus.
-Present in blood stream for days to years.
-Limited life spans requires constant replacement by bone marrow stem cells
cytoplasmic fragments of a bone marrow-bound cell
Present in blood stream for 10 days
1. biconcave (dumbbell-shaped), anucleated disc with 1/3 central pallor.
2. small cell diameter of ~7.5 M but w/ a large surface area.
3. mostly a "bag" full of hemoglobin (Hb) protein (97%) since nucleus & organelles are lost prior to bone marrow release.
4. cytoskeletal structural proteins like spectrin maintain shape while also allowing for cell flexibility in small spaces.
four covalently-linked polypeptide chains each with a bound heme group
four nitrogen-containing protoporphyrin rings each w/ one central iron (Fe) atom
Hemoglobin oxyhemoglobin (Hb:O2)
oxidized form, Hb combined with O2
oxygen loading (saturation) takes place in lungs
Hemoglobin deoxyhemoglobin (Hb:_)
- reduced form, no associated O2
short-lived form occurring in between oxyhemoglobin releasing its bound oxygen & subsequent binding of CO2 for return trip
Hemoglobin carbaminohemoglobin (Hb:CO2)
Hb bound to carbon dioxide
carbon dioxide loading takes place in tissue spaces
Hemoglobin carboxyhemoglobin (Hb:CO)
Hb bound to available carbon monoxidestable
stable union prevents O2 release to tissues
Hematopoietic stem cells
are self-renewing cells that are "signaled" by cytokines to produce each cell line
immature stem cells
divide several times to produce progenitors, which further differentiate into mature (effector) cells
make cells "commit" to one of two major cell lines: lymphoid stem cells or myeloid stem cells
lymphoid stem cells
produce only lymphocytes
myeloid stem cells
produce RBC, platelets, & all other leukocytes
Erythrocyte (RBC) Production
maintenance requires new cell production = old cell destruction
growth/repair requires new cell production > old cell destruction
Production requirements for Erythrocyte (RBC) Production
1. adequate iron (Fe) supply
2. adequate amino acids for Hb production
3. B vitamins for DNA synthesis
4. release of kidney erythropoetin (EPO), as required
cannot synthesize new proteins like cytoskeletal spectrin (no nucleus = no DNA blueprint)
Aging effects of RBC
-Membranes become increasingly inflexible (rigid)/fragile & are easily damaged when passing through reticular tissues (spleen).
-Hb starts to degenerate → less O2-carrying capacity
engulf "old" RBCs breaking Hb down into heme & globin fractions
Fe is recovered, nitrogen ring waste is converted into bilirubin by liver then excreted
eventually reduced to amino acids
due to excessive blood loss
Fe-deficiency, pernicious anemias
nutritional deficiency of either Fe or vitamin B12, respectively
deficiency of kidney-produced erythropoietin
excessive/early RBC destruction
inadequate production of either α or -chains
genetically-altered (defective) Hb chains
abnormal, immature RBCs
Leukocytes (WBCs) Characteristics
All mature WBCs have a nucleus (only complete blood cells).
Normally < 1% of blood volume (RBC/WBC ratio = 1,000:1).
1 degree of cellular defense mechanisms are either phagocytosis or antibody (Ab) production
Leukocytes (WBCs) body locations
Some leave bloodstream migrating to tissues where they take up residence
Others remain in blood/bone marrow until recruited to inflammatory sites by other WBCs releasing chemotaxins (chemical signals)
Total WBC count
determines total number of leukocytes in a volume of blood regardless of type
detects relative number (%) of each leukocyte type by counting 100 cells
- distinct granules are seen in cell cytoplasm
-neutrophils (neutral staining)
-no apparent granules in cell cytoplasm
-monocytes (single large nucleus)
lymphocytes (little cytoplasm)
mature form has multi-segmented nucleus w/ several nuclear lobes
destroy/digest ingested microorganisms (e.g. bacteria, fungi) via a respiratory burst
contains large, uniform-sized orange-red cytotoxic granules
attack parasitic worms, phagocytize antibody-antigen complexes
contain large, dark purple, variable-sized granules containing inflammatory agents
mediate inflammatory/allergic rxns
largest WBC, single nucleus w/ a large amount of grayish-blue cytoplasm
destroys microbes/removes dead tissue cells either as a "housekeeping" function or following infections/trauma
large dense nucleus, little cytoplasm
non-phagocytic immune responders
- small cell fragments released by bone marrow-bound megakaryocytes
- bleeding control
decrease total WBC numbers to <4,000 cells per µL
↑ total WBC numbers to >11,000 cells per µL
soft tissue tumor of myeloid cells
solid tissue tumor of lymphoid cells
localized process to quickly stop bleeding when blood vessel endothelium are lost/disrupted
endothelial cell death
expected event in otherwise intact blood vessels, results in decrease of blood loss
-cells are released from underlying basement membrane collagen fibers, leaves gaps (holes) in a vessel wall
endothelial cell disruption
unexpected event due to vessel disruption, results in increase of blood loss
-usually of traumatic origin (disease/wounds), may also destroy basement membrane
Major components of Hemostasis
1. blood vessels (endothelium)
2. platelets (thrombocytes)
3. coagulation proteins (circulating)
Intact endothelial cells
secrete prostacyclin, which inhibits platelet activation/aggregation
allows platelets to:
1. adhere to exposed underlying basement membrane collagen fibers
2. activate/release platelet aggregation promoters like ADP
initial (1) vascular spasm is followed by (2) let plug formation.
-occurs in all vessel types, forms a platelet plug
-Always takes place!
cascade activation of coagulation (3) proteins causes stabilization of a platelet plug (blood clot)
-occurs in higher pressure arteries/arterioles, stabilizes platelet plug
-only takes place when its necessary!
platelets release a potent vasoconstrictor (serotonin) causing blood vessel smooth muscle contraction
platelet plug formation
underlying basement membrane collagen fibers are exposed when endothelium is lost
Platelet Plug Formation
-platelet plug formation
-platelets adhere to exposed collagen & also stick to each other
-collagen-bound platelets releases cytoplasmic granules to recruit more platelets to affected area
-newly recruited platelets release more granules creating a positive feedback loop
-platelet plug seals gap but stops when it reaches adjacent intact endothelium*
(Secondary hemostasis) localized sequential activation of circulating soluble proteins produce an insoluble protein*
accelerate (+) or decelerate (-) thrombin formation
Secondary Hemostasis Requirements
-ionized Ca2+ - adequate levels
-coagulation proteins (factors I-XII) - circulating plasma proteins (liver origin), must be activated
-regulatory enzymes - accelerate (+) or decelerate (-) thrombin formation
enzymatic breakdown of blood clots when blood vessel repair has been completed (new endothelium).
-required to re-establish 100% local circulatory capacity
-previously incorporated* plasminogen (inactive) is enzymatically cleaved to plasmin (active)
-occurs by endothelium releasing tissue plasminogen activator (tPA)
a stationary, stabilized blood clot formed along a vessel wall w/o obstruction, non-occlusive event. Blood keeps flowing but not at 100%
a stationary blood clot that obstructs/blocks blood flow through a blood vessel, occlusive event
freely moving (detached) solid, liquid, or gas material in bloodstream, lodges in a smaller vessel
moving blood clot, blocks blood flow in vessels smaller than where its formed
substances used to suppress and/or prevent blood clotting after a heart attack, stroke, deep vein thrombosis (DVT), pulmonary embolism (PE)
anti-thrombotic agents (drugs)
low-dose aspirin (40-100 mg) blocks platelet enzyme synthesis ↓ platelet aggregation
- injected substances to dissolve formed clots by activating plasminogen
biological force pump maintaining blood circulation (movement) both to & from body tissues
-compresses blood (fluid) in heart chambers forcibly ejecting it
-maintains rhythmic contraction at desired time intervals
Cardiovascular (circulatory) system
closed system where blood is flows through intact circulatory vessels
-components = heart + blood vessels + blood
-O2/nutrient delivery w/ CO2/waste removal
Any blood vessel that carries blood away from the heart. No matter the oxygen concentration.
Any blood vessel that carries blood back to the heart. No matter the oxygen concentration
pulmonary circuit pump
right heart blood moves only to-and-from lungs
systemic circuit pump
- left heart blood supplies all body tissues/organs (includes lungs)
-size approximates a human adult fist
-weight is < 16oz (250-350 grams)
-located in mediastinum (medial thoracic cavity) extending from 2nd -5th rib level
-contacts diaphragm superior surface
-2/3 is located left of body midline
-flanked on either side by lungs
-anterior to vertebral column, posterior to sternum
double-walled sac around heart muscle
loose fitting, outer single tough connective tissue layer
-anchors major heart blood vessels
-prevents heart overfilling
slippery, inner two-layer connective tissue membrane lying deep to fibrous pericardium
outer membrane portion facing fibrous pericardium, attached to large superior arteries leaving heart
visceral layer (epicardium)
inner membrane portion facing heart surface, also part of heart wall
intervening fluid-filled space to reduce friction during contraction, contains pericardial fluid
Three layers of heart wall
epicardium (visceral pericardium)
innermost layer of serous pericardium, directly contacts underlying heart muscle
middle layer of contracting, interconnected cardiac muscle arranged in circular bundles, bulk of heart
endothelial layer lining inner portion of heart chambers & valves
dense network of crisscrossing, interlacing fibrous (collagen) connective tissue bundles
Cardiac skeleton functions
1. reinforces internal myocardium
2. anchors cardiac muscle fibers (acts as both tendon & insertion)
3. supports heart valves/major vessels (thicker in these areas)
4. limits action potential (AP) spread
partition marking L/R chamber boundaries
divides ventricles (not at midline)
depression marking chamber boundary
coronary sulcus (AV groove)
divides atrium from its ventricle
anterior interventricular sulcus
divides L/R ventricles anteriorly
posterior interventricular sulcus
divides L/R ventricles posteriorly
heart receiving chambers
small protruding tissue, marks atrium border
small ridges of cardiac muscle in atrial walls
depression marking area of open communication between L/R atria during fetal development (closes before birth)
heart discharging chambers, L is larger than R
holds valves during ventricular contraction*
trabeculae carneae muscles
irregular ridges of cardiac muscle marking ventricular walls, forces blood out during contraction
Venous blood flow (CO2-rich)
vena cavea right atrium (RA) to tricuspid valve (TV) to right ventricle (RV) to pulmonary semilunar valve (PSV) to pulmonary arteries (PA) to lungs
Arterial blood flow (O2-rich)
pulmonary veins (PV) to left atrium (LA) to bicuspid valve (BV) to left ventricle (LV) to aortic semilunar valve (ASV) to aorta to systemic circulation
provides functional blood supply to all heart muscle layers
collateral channels providing alternate blood routes during episodes of blockage
maintains O2 perfusion during coronary artery blockage (occlusion)
flexible edocardium flaps reinforced by connective tissue, ensures unidirectional blood flow
Atrioventricular (AV) valves
prevents blood backflow into atria during ventricular contraction
1. bicuspid (mitral) valve = left AV valve
2. tricuspid valve = right AV valve
thread-like bands of fibrous tissue anchoring AV valves to papillary muscles
small muscle bundles attached to chordea tendineae, tighten during ventricular contraction
prevent blood backflow into ventricles from major vessels after ventricular contraction
1. aortic semilunar* valve - located between left ventricle/aorta
2. pulmonary semilunar valve - located between right ventricle/pulmonary trunk
excitation-contraction coupling occurs as a depolarization wave passes to adjacent myocardial cells through gap junctions
allows cells to act as a functional syncytium contracting in unison
Intrinsic Conduction System
Autorhythmic cardiac cells or pacemaker cells control cardiac muscle depolarization & subsequent contraction
sinoatrial (SA) node
normal heart pacemaker, usually found in upper wall of right atrium
"sets" heart resting contraction rate by generating ~70-75 impulses per minute
Excitation Sequence (Normal)
1 SA node generates a pacemaker impulse (AP) that moves quickly towards AV node & also left atrium
2 AV node receives SA node impulse after a 0.1s delay, which allows enough time to depolarize left atrium*
3 AV bundle (bundle of His) receives impulse from AV node
4 AV bundle splits into bundle branches, traveling through interventricular septum carrying an impulse towards heart apex
5 highly branched Purkinje fibers carry impulses deep into heart apex & also towards outer ventricular walls
excitable group of cells located outside of a normally functioning SA node that cause abnormal heart beats
premature ventricular contraction (PVC)
a type of ectopic focus located in a ventricle, causes abnormal ventricular contractions
AV node "takes over" pacing due to damaged SA node but does so at 40-60 beats/min (bpm)
conduction impulses are slowed/disrupted as they move through heart decreasing rate to 30-40 bpm, arrhythmia
occurs at any conduction level, classified as 1st-3rd degree (worst)
small, implanted pulse generator w/ leads (1) senses heart activity (2) conducts impulses
on-demand only takes over to correct an arrhythmia
transcutaneous external cardiac pacing (TEPs)
temporary pacing used before/after cardiac surgery
surgical scarring/destroying of ectopic focus tissue, usually done by catheter insertion into affected area
extrinsic ANS cardiac control center w/ ANS fibers extending to heart SA/AV nodes
sympathetic fibers increase rate/force
parasympathetic fibers decrease rate/force
instrument used to measure electrical changes in heart activity
composite graph of all heart nodal + myocardium AP's (impulses)
beginning of atrial excitation to beginning of ventricular excitation
completion of ventricular depolarization
beginning of ventricular depolarization through ventricular repolarization
1. overall heart conduction rate
2. deflection wave shape, height*, duration
3.pattern deviations from normal
process of using a stethoscope to detect heart sounds.
pattern of heart contractions
extra or unusual heart sounds* heard during a heartbeat, result from an interruption of blood flow (turbulence)
valves do not completely close so blood regurgitates from ventricle back into atrium (clicking sound)
narrowed, thickened, or stiffened valves restrict blood flow (harsh/rough sound w/ thrill or vibration)
extra heart sound resulting from pericarditis
all events associated w/ blood flow during 1 complete heartbeat (atrial systole → ventricular diastole)
small dip in aortic pressure as some blood moves (rebounds) back towards left ventricle as aorta recoils
happens because the semilunar valve closes.
total blood volume (ml) pumped out of each ventricle in 1 minute (60 seconds)
heart rate (HR)
number of heartbeats per unit time (beats/min)
difference between resting CO & a maximal CO
amount of blood one ventricle pumps out during a single beat.
end diastolic volume (EDV)
blood volume at end ventricular loading (diastole)
end systolic volume (ESV)
blood volume remaining in ventricles after ventricular contraction (systole)
degree of stretch of cardiac muscle cells before they contract or EDV ( increase stretch = increase fillingincreased= EDV)
contractile strength of cardiac muscle can be increased, which results in ↓ ESV
aortic pressure that must be overcome by ventricular pressure to eject blood, resistance by blood in systemic circuit